Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Cell Immunol. 2024 Sep-Oct;403-404:104856. doi: 10.1016/j.cellimm.2024.104856. Epub 2024 Jul 10.
Yersinia pestis is the causative agent of bubonic, septicemic and pneumonic plague. The historical importance and potential of plague to re-emerge as a threat worldwide are indisputable. The most severe manifestion of plague is pneumonic plague, which results in disease that is 100% lethal without treatment. Y. pestis suppresses host immune responses early in the lung to establish infection. The later stages of infection see the rapid onset of hyperinflammatory responses that prove lethal. The study of Y. pestis host/pathogen interactions have largely been investigated during bubonic plague and with attenuated strains in cell culture models. There remains a somewhat limited understanding of the interactions between virulent Y. pestis and immune populations in the lung that drive severe disease. In this review we give a broad overview of the progression of pneumonic plague and highlighting how Y. pestis interfaces with host innate immune populations in the lung to cause lethal disease.
鼠疫耶尔森菌是腺鼠疫、败血型鼠疫和肺鼠疫的病原体。鼠疫作为一种可能在全球范围内死灰复燃的威胁，其历史重要性和潜在威胁是不可否认的。鼠疫最严重的表现形式是肺鼠疫，如果不治疗，该病的死亡率为 100%。鼠疫耶尔森菌在肺部早期抑制宿主的免疫反应，从而建立感染。感染的后期阶段会迅速出现过度炎症反应，从而导致死亡。鼠疫耶尔森菌宿主/病原体相互作用的研究主要在腺鼠疫和细胞培养模型中的减毒菌株中进行。对于毒力鼠疫耶尔森菌与肺部免疫群体之间导致严重疾病的相互作用，人们的了解仍然相当有限。在这篇综述中，我们广泛概述了肺鼠疫的进展，并强调了鼠疫耶尔森菌如何与肺部的宿主先天免疫群体相互作用，导致致命疾病。
